Wednesday, August 18, 2010

Accessibility: Intermediate-Advanced

The human visual system includes two pathways, magnocellular and parvocellular, deriving from two types of retinal ganglion cells that project to different layers of the lateral geniculate nucleus. Generally speaking, the magnocelluar pathway is specialized for movement while the parvocellular pathway is specialized for color and detail. Some researchers have found dyslexia to be associated with magnocelluar impairment, although evidence has been mixed.

A paper from Sperling and colleagues argues that magnocelluar deficits in dyslexica may actually be a deficit in noise exclusion. The authors tested children with and without dyslexia using stimuli that were designed to activate the magnocellular or parvocellular pathways. The magnocellular stimulus was a patch with white bars that alternated rapidly between light and dark. The parvocellular stimulus had thin light and dark bars that did not alternate.

In addition to the two stimulus types, there was a high noise and low noise condition. In the low noise condition, one of the stimuli appeared to the left or right of the fixation mark. In the high noise condition, noise patches appeared on either side of fixation and the stimulus was overlaid onto one of the noise patches. In both cases, child had to say on which side the stimulus appeared.

The authors calculated contrast thresholds (the amount of contrast needed between the light and dark bars for accurate detection) for both groups of children. They found no difference in the contrast thresholds for the low noise condition. In the high noise condition, dyslexic children had higher contrast thresholds (more difficulty detecting) for both the magnocellular and parvocellular stimuli. In addition, thresholds in the high noise condition were correlated with language measures.

These are interesting results. While one study cannot rule out the magnocellular theory of dyslexia, this does open the possibility that many of the results that pointed to a magnocellular deficit were actually cases of noise exclusion deficit. I do remember one paper about motion perception and dyslexia that can't be explained by noise, so I'll see if I can write about that later.

Another question is, how does noise exclusion lead to dyslexia? It could be that a noise exclusion deficit results in difficulties building phonological categories, which in turn affect reading. The authors also mention that noise exclusion could affect learning in the visual modality by making it harder to extract regularities from different fonts and scripts.

Wednesday, August 4, 2010

Accessibility: Advanced/intermediate

Early research on the role of the occipitotemporal region in reading often focused on characterizing a single region in the mid fusiform, commonly called the visual word form area. Since then, focus has gradually shifted from a single region to the entire length of the occipitotemporal region, looking at how the sensitivity and tuning changes as you move from posterior to anterior regions.

Van der mark used an approach like this to look at dyslexic and control children aged 9-12 years. Eighteen normal reading and twenty four dyslexic children performed a phonological lexical decision task in the scanner. Children saw words, pseudohomophones (words that sounded like real words but spelled differently, like “taksi”), pseudowords (pronounceable nonwords), and false fonts. The children were asked to decide whether something sounded like a real word. For example, the correct response would be “yes” for words and pseudohomophones and “no” for pseudowords and false fonts.

The children with dyslexia did worse for pseudohomophones and pseudowords and performed similarly to the controls for words and false fonts.

The authors report two main findings. First, the control children showed a gradient of print specialization in the occipitotemporal region, with more activation to false fonts in posterior regions and more activation to real letters and anterior regions. The control children did not show this trend.

Second, control showed more activation for pseudowords and pseudohomophones than words, while children with dyslexia didn't.

This is a nice study that takes a more nuanced approach to dyslexia brain differences. Brem and colleagues also got similar results with the words and false fonts.

By now there's quite a bit of literature on the specialization of the visual word form area. My own struggle, as I’m also doing this type of research, is the question of what does it all mean? We have all the studies now showing brain differences between control and dyslexic children, but what does it mean to have more or less activation? That the brains of dyslexic children process words differently? I could've told you that before we stared.

So what would help? Perhaps the next step in dyslexia research, now that we've mapped out the basic differences, is to zoom in as much as we can on the relationships between brain differences and behavioral differences. Perhaps more fine grained behavioral measures would help, or more interventional studies that looked at brain activation before and after training. It may also help to look at functional connectivity and how different brain regions interact. Anyone else have ideas?